[Buruli ulcer. A case report]. / L'ulcera di Buruli. Caso clinico.

The authors report a case of skin infection, Buruli ulcer, which is widespread in several parts of Africa: Ghana, Uganda, Ivory Coast, Senegal and most central African countries. This infection is caused by Mycobacterium ulcerans which belongs to the non-tubercular species Mycobacterium. It resembles Mycobacterium tuberculosis in colour and morphology, but differs in its speed of growth, its nutritional requirements, its capacity to produce pigments with enzymatic activities, its heat sensitivity and its resistance to anti-tubercular agents. Mycobacterium infection follows the percutaneous inoculation of the latter and appears as a painless, erythematous nodule that develops central necrosis and ulceration. Initially, the lesion appears as skin necrosis leading to the ulceration of the dermis and epidermis. The histological lesion shows a coagulative necrosis of the deep dermis and epidermis with destruction of the nerves and blood vessels; interstitial edema is also present. Healing is accompanied by a granulomatous response and the affected area is generally covered by a depressed scar. The authors initially treated the case in question using a conservative approach. A gel (Intrasite Gel) was used whose properties allowed the destruction of necrotic tissue present on the ulcer bed and the stimulation of granulation tissue formation. The layer of gel was in turn covered with a triple layer of polyurethane which enabled the humidity of the lesion to be maintained constant, thus promoting healing and acting as a barrier against external germs. This treatment enabled the skin lesion to be completely sterilised in about 30 days using new dressings every 3 days. Surgical treatment then led to complete healing after a further 20 days.

Modification of actin in peritoneal macrophages after diazepam treatment.

We have investigated the effect of therapeutic doses of diazepam (7 micrograms/mouse) on the association of actin with the macrophage cytoskeleton using cytochemical and morphological methods. Results obtained indicated that diazepam was able to modulate the content of actin in macrophages; such an effect proved to be time-dependent. After fixation and staining for indirect immunofluorescence with actin antibody, peritoneal macrophages from mice treated for short time with diazepam, showed a fluorescent intensity increase compared to control mice. The fluorescent intensity augmented reaching peak value within 14 days of treatment. Afterwards, this value dropped below control value for mice that underwent longer treatments. In the in vitro experiments concentrations of 10(-5) M, diazepam inhibited a well cell spread and a lower amount of actin after 15 min of incubation was also revealed. These results suggest that administration of diazepam in vivo plays a role in both the nonspecific and specific immune response, producing in the macrophages a reorganization process of microfilaments.

Effect of low-nutrient seawater on morphology, chemical composition, and virulence of Salmonella typhimurium.

The response of Salmonella typhimurium to low nutrient levels was determined by measuring the concentrations of lipids, carbohydrates, DNA, RNA, and proteins over a 32-day starvation period. Ultrastructural integrity was observed by transmission electron microscopy. Lipid and carbohydrate content of bacterial cells rapidly declined within the first 16 days, while DNA and proteins exhibited a more gradual decline over the 32 days of starvation. In contrast, RNA content did not decrease appreciably upon nutrient starvation. Structural damage occurred especially after 16 days of starvation. After 32 days of nutrient deprivation, we recorded degenerative cellular forms, a coccoidal cell shape, a decrease in cellular volume, and the loss of the three-layered outer membrane. The morphological and structural alterations correlated with virulence in infected animals. We observed a decrease in virulence of S. typhimurium after 9, 16, and 32 days of starvation, reaching a maximal decrease after 32 days of nutrient deprivation. The decrease in virulence correlated to surface hydrophobicity alterations, adherence to eukaryotic cells, and phagocytosis.